Abstract
This article reviews the types and roles of voltage-independent Ca 2+ channels involved in the endothelin-1 (ET-1)-induced functional responses such as vascular contraction, cell proliferation, and intracellular Ca 2+-dependent signaling pathways and discusses the molecular mechanisms for the activation of voltage-independent Ca 2+ channels by ET-1. ET-1 activates some types of voltage-independent Ca 2+ channels, such as Ca 2+-permeable nonselective cation channels (NSCCs) and store-operated Ca 2+ channels (SOCC). Extracellular Ca 2+ influx through these voltage-independent Ca 2+ channels plays essential roles in ET-1-induced vascular contraction, cell proliferation, activation of epidermal growth factor receptor tyrosine kinase, regulation of proline-rich tyrosine kinase, and release of arachidonic acid. The experiments using various constructs of endothelin receptors reveal the importance of G q and G 12 families in activation of these Ca 2+ channels by ET-1. These findings provide a potential therapeutic mechanism of a functional interrelationship between G q/G 12 proteins and voltage-independent Ca 2+ channels in the pathophysiology of ET-1, such as in chronic heart failure, hypertension, and cerebral vasospasm.
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